Disseminated Mycobacterium simiae infection in a patient with adult-onset immunodeficiency due to anti-interferon-gamma antibodies - a case report.

BACKGROUND: Mycobacterial species other than Mycobacterium tuberculosis and Mycobacterium leprae are generally free-living organisms and Mycobacterium simiae is one of the slowest growing Non-tuberculous mycobacteria. This is the first case report of Mycobacterium simiae infection in Sri Lanka and only very few cases with extrapulmonary manifestation reported in the literature. CASE PRESENTATION: A 24-year-old, previously healthy Sri Lankan male presented with generalized lymphadenopathy with discharging sinuses, evening pyrexia, weight loss, poor appetite and splenomegaly. Lymph node biopsies showed sheets of macrophages packed with organisms in the absence of granulomata. Ziehl Neelsen, Wade Fite and Giemsa stains revealed numerous red coloured acid-fast bacilli within foamy histiocytes. Slit skin smear for leprosy was negative and tuberculosis, fungal and bacterial cultures of the lymph node and bone marrow did not reveal any growth. Later he developed watery diarrhea and colonoscopy revealed multiple small polyps and ulcers throughout the colon extending up to the ileum, Which was confirmed to be due to cytomegalovirus confirmed by PCR and successfully treated with ganciclovir. Positron emission tomography scan guided biopsies of the gut and lymph nodes confirmed presence of mycobacterial spindle cell pseudo-tumours and PCR assays revealed positive HSP65. The culture grew Mycobacterium Simiae. Flow cytometry analysis on patient's blood showed extremely low T and B cell counts and immunofixation revealed low immunoglobulin levels. His condition was later diagnosed as adult onset immunodeficiency due to anti- interferon - gamma autoantibodies. He was initially commenced on empirical anti-TB treatment with atypical mycobacterial coverage. He is currently on a combination of daily clarithromycin, ciprofloxacin, linezolid with monthly 2 g/kg/intravenous immunoglobulin to which, he had a remarkable clinical response with complete resolution of lymphadenopathy and healing of sinuses. CONCLUSIONS: This infection is considered to be restricted to certain geographic areas such as mainly Iran, Cuba, Israel and Arizona and this is the first case report from Sri lanka. Even though the infection is mostly seen in the elderly patients, our patient was only 24 years old. In the literature pulmonary involvement was common presentation, but in this case the patient had generalized lymphadenopathy and colonic involvement without pulmonary involvement.

Scleredema associated with immunoglobulin A-κ smoldering myeloma: a case report and review of the literature.

BACKGROUND: Scleredema is a rare sclerodermoid skin condition characterized by diffuse symmetrical thickening of the upper part of the body. Its association with monoclonal gammopathy and myeloma was recently described; very few cases have been reported to date. CASE PRESENTATION: A 66-year-old Sri Lankan woman who had been followed in a dermatology unit for 34 years with diffuse systemic sclerosis presented with an acute exacerbation of the skin disease. Absence of Raynaud's phenomenon; sclerodactyly; characteristic lung, gastrointestinal, and cardiac involvement of systemic sclerosis; and repeatedly negative antinuclear antibodies test results led to reevaluation for the possibility of scleredema. Skin biopsies from four body sites showed normal epidermis and thickened reticular dermis with swollen collagen bundles separated from one another by clear spaces, resulting in fenestration. The skin appendages were not atrophied or bound down. Alcian blue staining showed interstitial mucin deposition. Serum protein electrophoresis demonstrated an abnormal monoclonal band in the ß-region with a paraprotein level of 8.9 g/dl. Immunofixation showed an abnormal band in the γ-region consisting of immunoglobulin A and κ. Bone marrow biopsy revealed abnormal monoclonal plasma cells (15%) with multinuclearity. There was no evidence of end organ damage, and whole-body magnetic resonance imaging did not reveal any evidence of bone involvement. The patient's diagnosis was revised as scleredema type 2 associated with IgA-κ, and she was referred to a hemato-oncologist for chemotherapy, which led to significant improvement in the skin condition. CONCLUSIONS: Scleredema is a rare disorder that has an enigmatic, rare association with monoclonal gammopathy. Dermatologists should be aware of this rare but important association.

Knowledge, attitudes and skills in melanoma diagnosis among doctors: a cross sectional study from Sri Lanka.

OBJECTIVES: This study aimed to assess the knowledge, attitudes and skills of non-specialist doctors on timely referral of suspicious lesions for melanoma diagnosis. RESULTS: One hundred and twenty-three doctors (mean age; 30.4 years, SD ± 8.015) were enrolled. Very few (3.3%) correctly stated all four types of melanoma. Only 8.1% of the total sample had been trained to perform a total body examination for skin cancer detection and a majority (110/123) had never performed one. Almost all (95.2%) were not confident in using a dermatoscope for examination of a skin lesion. Only 17.9% of participants had discussed skin cancer/melanoma risk reduction with patients. Only 13.8% had educated at least one patient regarding skin self-examination for suspicious skin lesions. Knowledge and clinical skills regarding melanoma recognition was unsatisfactory in our sample. Urgent attention is needed to bridge the gap in knowledge and clinical skills on this topic.

A case report of giant pancreatic pseudocyst following acute pancreatitis: experience with endoscopic internal drainage.

BACKGROUND: Pancreatic cysts are being diagnosed more frequently because of the increasing usage of imaging techniques. A pseudocyst with the major diameter of 10 cm is termed as a giant cyst. Asymptomatic pseudo-cysts up to 6 cm in diameter can be safely observed and monitored without intervention, but larger and symptomatic pseudocysts require intervention. CASE PRESENTATION: A 27-year-old Sri Lankan male, with history of heavy alcohol use, presented with progressive abdominal distension following an episode of acute pancreatitis. Contrast enhanced CT scan of the abdomen showed a large multilocular cystic lesion almost occupying the entire abdominal cavity and displacing the liver medially and the right dome of the diaphragm superiorly. The largest locule in the right side measured as 30 cm × 15 cm × 14 cm. Endoscopic ultrasound guided drainage of the cyst was performed. The cyst was entered into with an electrocautery-assisted cystotome and a lumen-opposing metal stent was deployed under fluoroscopic vision followed by dilatation with a 10 mm controlled radial expansion balloon. Repeat endoscopic ultrasound was done a week later due to persistence of the collection and a second stent was inserted. Then 10 French gauge × 10 cm double ended pigtails were inserted through both stents. The cysts were not visualized on subsequent Ultra sound scans. Stent removal was done after 3 weeks, leaving the pigtails insitu. The patient made an uneventful recovery. CONCLUSION: Giant pancreatic pseudocysts are rare and earlier drainage is recommended before clinical deterioration. Some experts suggest that cystogastrostomy may not be appropriate for the treatment of giant pancreatic pseudocysts and in some instances external drainage of giant pancreatic pseudocysts may be safer than cystogastrostomy. Video-assisted pancreatic necrosectomy with internal drainage and laparoscopic cystogastrostomy were also tried with a good outcome. With our experience we suggest endoscopic guided internal drainage as a possible initial method of management of a giant pseudo cyst. However long-term follow up is needed with repeated imaging and endoscopy. In instances where the primary endoscopic internal drainage fails, surgical procedures may be required as a second line option.

Erythroderma and extensive poikiloderma - a rare initial presentation of dermatomyositis: a case report.

BACKGROUND: Dermatomyositis is a humoral-mediated inflammatory myopathy with symmetrical proximal muscle weakness and dermatological manifestations such as Gottron's papules, heliotrope rash, periungual abnormalities, and flagellate erythema. Erythroderma is a severe and potentially life-threatening dermatological condition with diffuse erythema and scaling involving more than 90% of the skin surface area. Poikiloderma vasculare atrophicans refers to mottled hyperpigmentation and hypopigmentation of the skin with in-between telangiectases and areas of atrophy and is considered a variant of mycosis fungoides. Poikilodermatomyositis is the term given to the condition with poikiloderma and inflammatory myopathy. Only a few cases are reported on erythroderma in dermatomyositis and poikilodermatomyositis. Erythrodermal pattern of dermatomyositis transforming into poikilodermatomyositis is a recognized rare manifestation of dermatomyositis and we could find only one case report in the literature. CASE PRESENTATION: A 53-year-old Sri Lankan woman presented with intermittent fever of 5 months' duration with erythroderma. Later she developed progressive, symmetrical proximal muscle weakness. Following a short course of small dose steroids, erythroderma settled but changed to extensive poikiloderma involving more than 90% of her skin with her face being relatively spared. She had an early heliotrope rash, shawl sign, and Gottron papules. Electromyography and muscle biopsy were supportive of inflammatory myositis and skin biopsy showed evidence of dermatomyositis. Inflammatory markers and muscle enzymes were also elevated. Autoimmune antibodies and myositis-specific autoantibodies were negative. She was started on orally administered prednisolone 1 mg/kg per day with methotrexate 10 mg once a week and had a good response to treatment with resolution of the skin condition and improvement of muscle power. Imaging studies, endoscopies, and tumor markers did not reveal any malignancy. CONCLUSIONS: This case illustrates a rare presentation of dermatomyositis initially presenting as fever, erythroderma, and proximal muscle weakness and later developing poikiloderma involving more than 90% of the skin. It is important to be aware of this rare presentation to avoid misdiagnosis. With the currently available literature it is not possible to conclude that erythroderma is a bad prognostic factor in dermatomyositis or a predictive factor for a malignancy. Patients have a good response to steroids with a combination of immunosuppressants.

A case of anterior spinal cord syndrome in a patient with unruptured thoracic aortic aneurysm with a mural thrombus.

BACKGROUND: Spinal cord infarction is an uncommon condition. Anterior cord syndrome present with paraparesis or quadriparesis with sparing of vibration and proprioceptive senses. The common causes of anterior cord syndrome are aortic dissection and aortic surgical interventions. Spontaneous unruptured nondissected aortic aneurysms with intramural thrombus can rarely cause anterior cord infarctions. CASE PRESENTATION: We report a case of anterior spinal cord syndrome due to aneurysm of the thoracic aorta with a mural thrombus. A 64 year old male presented with sudden onset paraparesis with a sensory level at T1 with preserved sense of proprioception and vibration. The MRI panspine revealed increased T2 intensity in the anterior portion of the spinal cord from C5 to T10 level with characteristic 'owl eye' appearance on axial imaging. The CT aortogram detected aneurysmal dilatation of the ascending aortic, arch and descending thoracic aorta with significant intimal irregularities, calcified atherosclerotic plaques and a small mural thrombus. CONCLUSION: The possible mechanisms postulated are occlusion of ostia of radicular arteries by the atherosclerotic plaques and mural thrombus or thromboembolism to the anterior spinal artery. Nondissected atherosclerotic aortic aneurysms should be considered in patients presenting with spinal cord infarctions especially in the presence of vascular risk factors and smoking.

Opsoclonus myoclonus syndrome in a patient with Japanese encephalitis: a case report.

BACKGROUND: Opsoclonus myoclonus syndrome is a rare neurological disorder that usually manifests as a paraneoplastic phenomenon. Although some viruses are reported to cause this condition, opsoclonus myoclonus syndrome by Japanese encephalitis has not been reported previously. CASE PRESENTATION: Here we present the case of a 31-year-old Sri Lankan woman who presented with fever, altered level of consciousness, opsoclonus, and facial myoclonus. She was diagnosed as having Japanese encephalitis based on cerebrospinal fluid and serum Japanese encephalitis-specific immunoglobulin M antibody and characteristic magnetic resonance imaging abnormalities. She was given intravenously administered methylprednisolone pulses (1000 mg per day) for 5 days. With this she improved gradually with reduction in opsoclonus and myoclonic movements. Her limb muscle power and speech also improved slowly. CONCLUSIONS: We intended to highlight the fact that opsoclonus myoclonus syndrome can be a feature of infection with Japanese encephalitis and that it can be added to the list of viruses which cause opsoclonus. Currently there is no well-accepted treatment for opsoclonus myoclonus syndrome and intravenously administered methylprednisolone pulses and immunosuppressants can be used successfully in these patients for early recovery.

Myocardial infarction during anaphylaxis in a young healthy male with normal coronary arteries- is epinephrine the culprit?

BACKGROUND: Anaphylaxis is an acute, potentially fatal medical emergency. Myocardial injury or infarction in the setting of an anaphylaxis can be due the anaphylaxis itself, when it is known as Kounis syndrome or it can also be due to the effect of epinephrine treatment. Epinephrine is considered as the cornerstone in management of anaphylaxis. Myocardial infarction secondary to therapeutic doses of adrenaline is a rare occurrence and only a few cases have been reported in literature. The mechanism of myocardial injury was considered to be due to coronary vasospasm secondary to epinephrine as the coronary angiograms were normal on these occasions. CASE PRESENTATION: A 21-year- old previously healthy male got admitted to the local hospital with an urticarial rash and difficulty in breathing, one hour after ingestion of prawns for which he was known to be allergic. He was treated with 0.5 ml of intramuscular adrenaline (1:1000) which was administered to the lateral side of the thigh, following which he developed palpitations and tightening type central chest pain. Electrocardiogram showed ST segment depressions in leads III, aVF and V1 to V5 and he was transferred to a tertiary care hospital. The second electrocardiogram, done 2 h later, showed resolution of ST segment depressions but new T inversions in leads I and aVL. Troponin I was elevated with a titer of 2.15 ng/ml. He was treated with sublingual GTN in the emergency treatment unit and the symptoms resolved. Transthoracic 2D echocardiogram and stress testing with treadmill was normal and CT coronary angiogram revealed normal coronary arteries. CONCLUSION: Here we present a case of a young healthy adult with no significant risk factors for coronary artery disease who developed myocardial infarction following intramuscular administration of therapeutic dose of adrenalin for an anaphylactic reaction. The postulated mechanism is most likely an alpha receptor mediated coronary vascular spasm. However the use of adrenaline in the setting of life threatening anaphylaxis is life saving and the benefits far outweigh the risks of adverse effects. Therefore the purpose of reporting this case is not to discourage the use of adrenaline in anaphylaxis but to make aware of this potential adverse effect which can occur in the acute setting.

Takotsubo cardiomyopathy complicated with apical thrombus formation on first day of the illness: a case report and literature review.

BACKGROUND: Takotsubo cardiomyopathy is characterized by transient systolic dysfunction of the apical and mid segments of the left ventricle in the absence of obstructive coronary artery disease. Intraventricular thrombus formation is a rare complication of Takotsubo cardiomyopathy and current data almost exclusively consists of isolated case reports and a few case series. Here we describe a case of Takotsubo cardiomyopathy with formation of an apical thrombus within 24 h of symptom onset, which has been reported in the literature only once previously, to the best of our knowledge. We have reviewed the available literature that may aid clinicians in their approach to the condition, since no published guidelines are available. CASE PRESENTATION: A 68-year-old Sri Lankan female presented to a local hospital with chest pain. Electrocardiogram (ECG) showed ST elevation, and antiplatelets, intravenous streptokinase and a high dose statin were administered. Despite this ST elevation persisted; however the coronary angiogram was negative for obstructive coronary artery disease. Echocardiogram revealed hypokinesia of the mid and apical segments of the left ventricle with typical apical ballooning and a sizable apical thrombus. She had recently had a viral infection and was also emotionally distressed as her sister was recently diagnosed with a terminal cancer. A diagnosis of Takotsubo cardiomyopathy was made and anticoagulation was started with heparin and warfarin. The follow up echocardiogram performed 1 week later revealed a small persistent thrombus, which had completely resolved at 3 weeks. CONCLUSION: Though severe systolic dysfunction is observed in almost all the patients with Takotsubo cardiomyopathy, intraventricular thrombus formation on the first day of the illness is rare. The possibility of underdiagnosis of thrombus can be prevented by early echocardiogram in Takotsubo cardiomyopathy. The majority of reports found in the literature review were of cases that had formed an intraventriclar thrombus within the first 2 weeks, emphasizing the importance of follow up echocardiography at least 2 weeks later. The management of a left ventricular thrombus in Takotsubo cardiomyopathy is controversial and in most cases warfarin and heparin were used for a short duration.

A case report of zinc phosphide poisoning: complicated by acute renal failure and tubulo interstitial nephritis.

BACKGROUND: Run Rat® is a rodenticide widely used against small mammals. It comprises of a minimum of 32% zinc phosphide which is highly toxic in acute exposures to humans. It may be consumed accidentally or intentionally. It enters the body via skin, respiratory and gastrointestinal tracts. Zinc phosphide is hydrolyzed by the gastric acid and is transformed into phosphine gas. Phosphine is a respiratory toxin that inhibits cytochrome C oxidase system resulting in renal failure and liver failure. CASE PRESENTATION: A 35 year old Sri Lankan female presented following ingestion of 2.5 g of Run Rat®, which is a branded preparation of zinc phosphide, resulting in 61 mg/kg poison load. She developed severe acute kidney injury with acute tubular necrosis, subnephrotic ranged proteinuria and tubulointerstitial nephritis for which she underwent haemodialysis three times along with other measures of resuscitation. She also developed elevated liver enzymes with hyperblirubinaemia, hypoalbuminaemia, acute pancreatitis and mild myocarditis. She improved with supportive therapy over a period of 3 weeks. CONCLUSION: Run Rat® is a commonly used rodenticide and the toxic effects are mediated through conversion of phosphide to phosphine gas. The majority of the deaths had occurred in the first 12 to 24 h and the main causes identified are refractory hypotension and arrhythmias. The late deaths (beyond 24 h) had been commonly due to adult respiratory distress syndrome, liver and renal failure. The outcome is poorer with delayed presentation, development of coagulopathy, hyperglycaemia and multiorgan failure with elevated liver enzymes. In our patient, Zinc phosphide poisoning caused severe acute kidney injury, abnormal liver profile, pancreatitis and possible myocarditis. The patient improved with repeated haemodialysis. The renal biopsy revealed acute tubulointerstitial nephritis with acute tubular necrosis. In tropical countries, the rural population engaged in agriculture has easier access to the compound, as it is available at a lower cost. Furthermore, the lack of an antidote and advanced resuscitative measures such as inotropic supportive therapy and renal replacement facilities at most of the peripheral hospitals pose a major challenge in providing timely interventions to prevent deaths.

Electrocardiographic changes mimicking acute coronary syndrome in a large intracranial tumour: A diagnostic dilemma.

BACKGROUND: ST elevation Myocardial infarction is a medical emergency. A variety of noncardiac conditions had been known to mimic the ECG changes that are seen in acute coronary syndrome. Although the common ECG changes that are documented with raised intracranial pressure are T inversions, prolongation of QT interval and sinus bradycardia, ST elevation or depression, arrhythmias and prominent U waves have also been recognized. However, ST elevations in association with primary intracranial tumours are rarely reported. CASE PRESENTATION: A 68-year-old female patient with a large left sided frontoparietal sphenoidal ridge meningioma with mass effect developed sudden onset shortness of breath while awaiting surgery. Her ECG showed ST segment elevations in the inferior leads along with reciprocal T inversions in anterior leads. The patient was treated with dual antiplatelet therapy and unfractionated heparin. The ST elevations in the ECG remained static and the cardiac Troponin assay was repeatedly negative. 2D ECHO, coronary angiogram and CT pulmonary angiography were normal. The repeat noncontract CT scan of the brain revealed two small areas of haemorrhage in the tumour. CONCLUSION: The two mechanisms for ECG changes described in subarachnoid haemorrhage are the neurogenic stunned myocardium due to the catecholamine surge on the myocytes and stress cardiomyopathy. The same mechanisms could be the reasons for the ECG changes seen in intracranial tumours. These ECG changes could be easily misdiagnosed as acute coronary syndrome. This case emphasizes the importance of the cardiac biomarkers, 2D ECHO and coronary angiogram when confronted with such a diagnostic dilemma. Thus a more holistic analysis should be practiced in diagnosing acute coronary events in patients with intracranial pathologies to obviate a myriad of unnecessary investigations, interventions, costly treatment strategies which may well be detrimental to the patient.

Large hepatocellular carcinoma in a non-cirrhotic liver with peritoneal and omental metastasis in a healthy man: a case report.

BACKGROUND: Liver cancer is the second leading cause of cancer death in men worldwide. Hepatocellular carcinoma usually develops in the setting of cirrhosis or chronic inflammation. Major risk factors for developing hepatocellular carcinoma are chronic hepatitis B or C virus infection, alcoholic cirrhosis, and nonalcoholic fatty liver disease. The most frequent locations for hepatocellular carcinoma to metastasize are the lungs, portal vein, bones, and regional lymph nodes. CASE PRESENTATION: A 41-year-old Sri Lankan man presented with progressive abdominal distension and on examination was found to have a palpable irregular mass in the left lobe of his liver with moderate ascites. His ascitic fluid was an exudate without malignant cells. An ultrasound scan and contrast-enhanced computed tomography of his abdomen showed a large contrast-enhancing lesion in the left lobe of his liver without features of cirrhosis. Laparoscopic assessment revealed peritoneal and omental deposits. Histology of the biopsies taken from the liver lesion, omental deposits, and peritoneal deposits supported a diagnosis of hepatocellular carcinoma. His liver biochemistry was normal and hepatitis serology was negative. He is abstinent from alcohol and did not have metabolic syndrome. CONCLUSIONS: It is rare for a young patient to develop hepatocellular carcinoma with a normal liver without chronic hepatitis B or C infection, or any other risk factors. Intraperitoneal metastasis of non-ruptured hepatocellular carcinoma is also very rare. Here we report a rare case of a 41-year-old man with a large hepatocellular carcinoma in a non-cirrhotic liver without chronic hepatitis who presented with peritoneal and omental metastasis.

Amitraz poisoning: A case report of an unusual pesticide poisoning in Sri Lanka and literature review.

BACKGROUND: Amitraz is a pesticide used worldwide on animals and in agriculture. It contains triazapentadiene, which is a centrally acting alpha-2 adrenergic agonist. Amitraz poisoning is fairly uncommon in humans and occurs via oral, dermal or inhalational routes. Only a limited number of case reports of human intoxication have been published and most of them are of accidental ingestion by children. CASE PRESENTATION: A twenty-year-old Sri Lankan female presented following self-ingestion of 20 ml of amitraz resulting in 37.8 mg/ kg of amitraz poisoning. She lost consciousness after 20 min of ingestion, developed bradycardia and hypotension, which needed intravenous fluid resuscitation and dobutamine. Gastric lavage was performed. Her bradycardia persisted for 36 h and she was drowsy for 48 h. She did not develop respiratory depression, convulsions or hypothermia and the urine output was normal. Arterial blood gas revealed mild respiratory alkalosis. She recovered fully within 48 h and was discharged on day 3. CONCLUSION: The clinical manifestations of amitraz (impaired consciousness, drowsiness, vomiting, disorientation, miosis, mydriasis, hypotension, bradycardia, respiratory depression, hypothermia, generalized seizures, hyperglycemia and glycosuria) can be explained by the agonist action of amitraz on α1 and α2 receptors. Management of amitraz poisoning is still considered to be supportive and symptomatic with monitoring of nervous system, cardiovascular and respiratory systems. Activated charcoal may still be considered for treatment and the place for gastric lavage is controversial. Atropine is effective for symptomatic bradycardia and inotropic support is needed for hypotension that does not respond to fluid resuscitation. Diazepam or Lorazepam is used for convulsions and some patients may require intubation and ICU care. Several α2 adrenergic antagonists like yohimbine have been tried on animals, which have successfully reversed the effects of amitraz. Since the majority of amitraz poisoning cases are due to accidental ingestion, manufactures, regulatory authorities and national poisons control centers have a significant role to play in minimizing its occurrence.

Acute pancreatitis complicated with deep vein thrombosis and pulmonary embolism: a case report.

BACKGROUND: Acute pancreatitis is an acute inflammatory process of the pancreas that can trigger a systemic inflammatory response. Pulmonary embolism refers to obstruction of the pulmonary artery or one of its branches by material (usually a thrombus) that originated elsewhere in the body. Extensive lower limb deep vein thrombosis with pulmonary embolism is a rare complication of acute pancreatitis that has been described in a few case reports. Deep vein thrombosis and hypercoagulable states in pancreatitis are thought to be due to release of pancreatic proteolytic enzymes from a cyst that is connected to the pancreatic duct and penetrates into a vessel. Proteolytic damage or inflammation of the vessels may also play a significant part. Acute pancreatitis also causes a systemic inflammatory response that has effects on an endothelium-dependent relaxing response for acetylcholine. CASE PRESENTATION: A 38-year-old Sri Lankan man presented with acute pancreatitis and later he developed progressive abdominal distention with bilateral ankle edema. A contrast-enhanced computed tomographic scan showed two pancreatic pseudocysts and deep vein thrombosis in both lower limbs, as well as a pulmonary embolism involving the right lower lobe pulmonary artery and the left segmental pulmonary arteries. One of the pseudocysts in the head of the pancreas was compressing the inferior vena cava without direct communication. The patient's thrombophilia screen result was negative. He was started on subcutaneous enoxaparin 1 mg/kg twice daily and warfarin to achieve a target international normalized ratio of 2-3. CONCLUSIONS: Deep vein thrombosis with pulmonary embolism is a rare but life-threatening complication of acute pancreatitis. Once diagnosed, early treatment with intravenous heparin or thrombolysis is effective. Patients with severe acute pancreatitis may be at risk of deep vein thrombosis due to immobilization and other mechanisms, but anticoagulation as prophylaxis is often not used. However, it may be considered on a case-by-case basis in patients with pancreatitis who are acutely ill and immobilized, need intensive care unit admission, and have multiple risk factors for deep vein thromboembolism. Further studies must be undertaken to determine guidelines for deep vein thromboembolism prophylaxis in these patients.